Purpose: This study aimed to characterize the clinical patterns and severity of brain injury in neonates who survived extracorporeal membrane oxygenation (ECMO) therapy for acute respiratory failure during the neonatal period, to evaluate their short-term neurodevelopmental outcomes, and to identify the factors associated with these outcomes. Methods: We retrospectively reviewed the medical records of neonates who survived ECMO between 2018 and 2024. Based on brain magnetic resonance imaging (MRI) findings, the patients were classified into two groups: no/mild and moderate/severe brain injury. Neurodevelopmental outcomes were assessed at 12–40 months of age using the Bayley Scale of Infant Development II/III and/or the Korean Developmental Screening Test. Results: Among the 19 neonates included in the study, 18 (94.7%) showed varying degrees of brain injury on MRI (mild: 12, moderate: 1, severe: 5). Neonates with moderate/severe brain injury had significantly longer durations of ECMO support and extended durations of mechanical ventilation and were more likely to receive continuous renal replacement therapy than those with no or mild injury. Developmental delay was identified in 36.8% of survivors and was significantly associated with prolonged mechanical ventilation, longer neonatal intensive care unit stays, and a higher incidence of seizures. Conclusion Brain injury is frequently observed on MRI in neonates treated with ECMO. However, its direct association with adverse neurodevelopmental outcomes is not definitive. Since MRI findings alone cannot predict developmental outcomes, clinical and environmental factors should be integrated into prognostic assessments.

Purpose: Congenital hypothyroidism (CH) is a major preventable cause of intellectual disability, particularly in very low birth weight (VLBW) infants, who are at increased risk due to hypothalamic-pituitary-thyroid axis immaturity. Early differentiation between transient CH (TCH) and permanent CH (PCH) is crucial to optimize L-thyroxine (LT4) treatment duration. This study aimed to determine the incidence of PCH among Korean VLBW infants and to identify clinical factors that may aid in distinguishing TCH from PCH. Methods: This retrospective cohort study included VLBW infants diagnosed with CH and treated with LT4 at a single tertiary neonatal intensive care unit between 2011 and 2020. Infants requiring LT4 beyond 3 years were classified as PCH, while those who discontinued earlier were considered TCH. Clinical characteristics, neonatal morbidities, and thyroid-related parameters were compared between the groups. Results: Among 1,292 VLBW infants, 122 (9.4%) were diagnosed with CH. After excluding deaths and those lost to follow-up, 73 infants were included in the final analysis (TCH, n=50; PCH, n=23). The PCH group had a significantly higher mean gestational age and greater LT4 requirements at both 12 and 36 months of age. Major anomalies were more frequently observed in PCH infants, including congenital heart defects. In multivariate analysis, higher gestational age, the presence of major anomalies, screening thyroid-stimulating hormone (TSH) >10 μIU/mL, and higher LT4 dose at 36 months were significantly associated with PCH. Conclusion The incidence of PCH in Korean VLBW infants was relatively higher than that reported in previous studies studies. Screening TSH level and LT4 dose requirements may support individualized follow-up and help distinguish PCH from TCH.

Purpose: This study aimed to characterize the clinical patterns and severity of brain injury in neonates who survived extracorporeal membrane oxygenation (ECMO) therapy for acute respiratory failure during the neonatal period, to evaluate their short-term neurodevelopmental outcomes, and to identify the factors associated with these outcomes. Methods: We retrospectively reviewed the medical records of neonates who survived ECMO between 2018 and 2024. Based on brain magnetic resonance imaging (MRI) findings, the patients were classified into two groups: no/mild and moderate/severe brain injury. Neurodevelopmental outcomes were assessed at 12–40 months of age using the Bayley Scale of Infant Development II/III and/or the Korean Developmental Screening Test. Results: Among the 19 neonates included in the study, 18 (94.7%) showed varying degrees of brain injury on MRI (mild: 12, moderate: 1, severe: 5). Neonates with moderate/severe brain injury had significantly longer durations of ECMO support and extended durations of mechanical ventilation and were more likely to receive continuous renal replacement therapy than those with no or mild injury. Developmental delay was identified in 36.8% of survivors and was significantly associated with prolonged mechanical ventilation, longer neonatal intensive care unit stays, and a higher incidence of seizures. Conclusion Brain injury is frequently observed on MRI in neonates treated with ECMO. However, its direct association with adverse neurodevelopmental outcomes is not definitive. Since MRI findings alone cannot predict developmental outcomes, clinical and environmental factors should be integrated into prognostic assessments.

Purpose: Congenital hypothyroidism (CH) is a major preventable cause of intellectual disability, particularly in very low birth weight (VLBW) infants, who are at increased risk due to hypothalamic-pituitary-thyroid axis immaturity. Early differentiation between transient CH (TCH) and permanent CH (PCH) is crucial to optimize L-thyroxine (LT4) treatment duration. This study aimed to determine the incidence of PCH among Korean VLBW infants and to identify clinical factors that may aid in distinguishing TCH from PCH. Methods: This retrospective cohort study included VLBW infants diagnosed with CH and treated with LT4 at a single tertiary neonatal intensive care unit between 2011 and 2020. Infants requiring LT4 beyond 3 years were classified as PCH, while those who discontinued earlier were considered TCH. Clinical characteristics, neonatal morbidities, and thyroid-related parameters were compared between the groups. Results: Among 1,292 VLBW infants, 122 (9.4%) were diagnosed with CH. After excluding deaths and those lost to follow-up, 73 infants were included in the final analysis (TCH, n=50; PCH, n=23). The PCH group had a significantly higher mean gestational age and greater LT4 requirements at both 12 and 36 months of age. Major anomalies were more frequently observed in PCH infants, including congenital heart defects. In multivariate analysis, higher gestational age, the presence of major anomalies, screening thyroid-stimulating hormone (TSH) >10 μIU/mL, and higher LT4 dose at 36 months were significantly associated with PCH. Conclusion The incidence of PCH in Korean VLBW infants was relatively higher than that reported in previous studies studies. Screening TSH level and LT4 dose requirements may support individualized follow-up and help distinguish PCH from TCH.

Objective: This study aims to investigate may moesin deficiency resulted in neurodevelopmental abnormalities caused by negative impact on synaptic signaling ultimately leading to synaptic structure and plasticity. Methods: Behavioral assessments measured neurodevelopment (surface righting, negative geotaxis, cliff avoidance), anxiety (open field test, elevated plus maze test), and memory (passive avoidance test, Y-maze test) in moesin-knockout mice (KO) compared to wild-type mice (WT). Whole exome sequencing (WES) of brain (KO vs. WT) and analysis of synaptic proteins were performed to determine the disruption of signal pathways downstream of moesin. Risperidone, a therapeutic agent, was utilized to reverse the neurodevelopmental aberrance in moesin KO. Results: Moesin-KO pups exhibited decrease in the surface righting ability on postnatal day 7 (p<0.05) and increase in time spent in the closed arms (p<0.01), showing increased anxiety-like behavior. WES revealed mutations in pathway aberration in neuron projection, actin filament-based processes, and neuronal migration in KO. Decreased cell viability (p<0.001) and expression of soluble NSF adapter protein 25 (SNAP25) (p<0.001) and postsynaptic density protein 95 (PSD95) (p<0.01) was observed in days in vitro 7 neurons. Downregulation of synaptic proteins, and altered phosphorylation levels of Synapsin I, mammalian uncoordinated 18 (MUNC18), extracellular signal-regulated kinase (ERK), and cAMP response element-binding protein (CREB) was observed in KO cortex and hippocampus. Risperidone reversed the memory impairment in the passive avoidance test and the spontaneous alternation percentage in the Y maze test. Risperidone also restored the reduced expression of PSD95 (p<0.01) and the phosphorylation of Synapsin at Ser605 (p<0.05) and Ser549 (p<0.001) in the cortex of moesin-KO. Conclusion Moesin deficiency leads to neurodevelopmental delay and memory decline, which may be caused through altered regulation in synaptic proteins and function.